Neuronal Basis of the Slow (In Vitro

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Abstract
During deep sleep and anesthesia, the EEG of humans and animals exhibits a distinctive slow (trans-ACPD [(+/−)-1-aminocyclopentane-trans-1,3-dicarboxylic acid] (50–100 μm) or DHPG [(S)-3,5-dihydroxyphenylglycine] (100 μm) instates an intrinsic slow oscillation in NRT neuronsin vitrothat is qualitatively equivalent to that observedin vivo. A slow oscillation could also be evoked by synaptically activating mGluRs on NRT neurons via the tetanic stimulation of corticothalamic fibers. Through a combination of experiments and computational modeling we show that the up state of the slow oscillation is predominantly generated by the “window” component of the T-type Ca2+current, with an additional supportive role for a Ca2+-activated nonselective cation current. The slow oscillation is also fundamentally reliant on anIhcurrent and is extensively shaped by both Ca2+- and Na+-activated K+currents. In combination with previous work in thalamocortical neurons, this study suggests that the thalamus plays an important and active role in shaping the slow (<1 Hz) rhythm during deep sleep.